A university study identifies a molecule that enhances fat burning

A study led by the University and the Hospital academic of Bonn (Germany) has identified a moleculethe purine inosine, which enhances fat burning in brown adipocytes. The mechanism, published in the scientific journal ‘Nature‘, was discovered in mice, but “probably” also exists in humans, according to Europa Press.

“If an inosine transporter is less active, the mice remain significantly Thinner despite a high-fat diet,” the agency reports. Normally, fat cells store energy. However, in brown fat cells, energy is dissipated as heat, so brown fat serves as a biological heater. For this reason, most of the mammals they have this mechanism that in humans keeps newborns warm; while in adults, the activation of brown fat is positively correlated with the cardiometabolic health.

We move less than our ancestors

“Today, however, we are well dressed even in winter. So our body’s own furnaces are hardly needed anymore. At the same time, we carry a diet increasingly energy dense and we also move much less than our ancestors. These three factors are poison to cells of brown fat: Little by little they stop working and end up dying. On the other hand, the number of people with severe overweight around the world continues to increase. Therefore, research groups around the world are looking for substances that stimulate brown fat and thus increase fat burning,” says Alexander Pfeiffer, one of the job managers.

Together with a group of colleagues, the team from the University of Bonn has now identified a key molecule called inosine that is capable of burning fat. “It is known that dying cells release a mixture of messenger molecules that influence the function of their neighbors. We wanted to know if this mechanism also exists in brown fat,” he details. Birte Niemannanother of the authors of the investigation.

Therefore, the researchers studied brown fat cells subjected to severe stress, so that the cells they practically died. “We found that they secrete the purine inosine in large amounts,” says Niemann.

What was most interesting, however, was how the intact brown fat cells responded to the molecular call for help: They were activated by inosine (or simply by the dying cells in their environment). Thus, the inosine fueled the fire within him. The cells of white fat they also became her brown sisters. Mice fed a high-energy diet and concurrently treated with inosine remained Thinner compared to control animals and were protected from diabetes.

Drug for coagulation disorders

The inosine transporter appears to play an important role in this context. This cell membrane protein transports inosine into the cell, thus reducing the extracellular concentration. Therefore, inosine can no longer exert its combustion-promoting effect. “There is a drug that was actually developed for coagulation disorders, but also inhibits the inosine transporter. We gave this drug to mice, and as a result, they burned more energy,” says Pfeifer.

Humans also have an inosine transporter. Two to four percent of people are less active due to genetic variation. “Our colleagues at the University of Leipzig have genetically analyzed 900 individuals. Subjects with the least active transporter were significantly Thinner on average,” explains Pfeifer. These results suggest that inosine also regulates the thermogenesis in human brown fat cells. Therefore, substances that interfere with transporter activity could be potentially suitable for the obesity treatment. The drug already approved for bleeding disorders could serve as a starting point.

“However, more studies in humans are needed to clarify the pharmacological potential of this mechanism,” says Pfeifer. He also doesn’t believe that a pill alone is going to be the solution to the obesity pandemic in the world. “But the available therapies are not effective enough at the moment. So we need desperately meds to normalize energy balance in obese patients,” he stresses.